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Biomedical subjects

A P Fishman

Publications and source records attributed to A P Fishman.

At least 91 records · Page 5Linked to original sources
PubMed1981

Influence of alterations in Starling forces on visceral pleural fluid movement.

The influence of alterations in hydrostatic and oncotic pressure gradients on fluid movement across the visceral pleura was examined in 16 spontaneously breathing anesthetized dogs. The left lung was enclosed in a water-impermeable polyethylene membrane, creating a visceral pleural space; visceral fluid movement was determined as the formation or reabsorption of fluid in this space. Aortic, pulmonary arterial, right and left atrial, and pleural pressures were monitored; oncotic pressure was calculated from the protein concentration of plasma and pleural fluid. Left atrial pressure was varied from 0 to 30 mmHg and pulmonary arterial pressure from 15 to 36 mmHg by inflating atrial balloon catheters; the plasma-to-pleural fluid oncotic gradient was varied from 6.8 to 19.3 mmHg by infusing saline. The movement of fluid across the visceral pleura was significantly (P less than 0.001) related to the effective (transmural hydrostatic pressure minus oncotic gradient) pulmonary arterial (r = 0.87) and left atrial pressures (r = 0.92). The filtration coefficient of the visceral pleura estimated by our technique was 1.1 x 10(-6) ml.s-1.cmH2O-1.cm-2. These results not only confirm the concept that fluid flux across the visceral pleura is determined by the action of Starling forces across this membrane but also provide an estimate of the filtration coefficient for the visceral pleura.

Animals↗
PubMed1981

Effects of hypercapnia and hypoxia on phrenic nerve activity and respiratory timing.

In the spontaneously breathing animal, respiratory responses to chemical stimuli are influenced by phasic proprioceptive inputs from the thorax. We have compared the effects of hypercapnia and hypoxia on the level and timing of phrenic nerve activity while these phasic afferent signals were absent. Progressive hyperoxic hypercapnia and isocapnic hypoxia were produced in anesthetized paralyzed dogs by allowing 3-5 min of apnea to follow mechanical ventilation with 100% O2 or 35% O2 in N2, respectively; during hypoxia, isocapnia was maintained by intravenous infusion of tris(hydroxymethyl)aminomethane buffer. The peak height (P) of nerve bursts, inspiratory time (TI), and expiratory time (TE) were measured from the phrenic neurogram. With the vagi intact or severed, hypoxia decreased TI, whereas hypercapnia did not; both stimuli decreased TE. At the same minute phrenic activity (P x frequency), P, TI, and TE were all less during hypoxia than during hypercapnia. The decreases in TI and TE with hypoxia were significantly less after carotid sinus denervation. The results indicate that the patterns of phrenic nerve activity in response to hypoxia and hypercapnia are different: hypoxia has a greater effect on respiratory timing, whereas hypercapnia has a greater effect on peak phrenic nerve activity. The effect of hypoxia on respiratory timing is largely mediated by the peripheral chemoreceptors.

Animals↗
PubMed1981

Effects of aging on ventilatory and occlusion pressure responses to hypoxia and hypercapnia.

Studies were performed to examine the decrease in ventilatory response to hypoxia and hypercapnia in the elderly and to explore its etiology. For this purpose, matched groups of normal elderly (65 to 79 yr of age) and young subjects were used. Standard pulmonary function tests were supplemented in both groups by determination of total respiratory compliance and the ventilatory responses to hyperoxic hypercapnia and isocapnic hypoxia using rebreathing methods. While testing the ventilatory responses, we recorded minute ventilation and its components, as well as mouth occlusion pressures, and rib cage and abdominal-diaphragmatic compartmental ventilation (magnetometry). We found that ventilatory responses to both hypercapnia and hypoxia were reduced in the elderly by approximately 50%. These reductions were not related to any change in control of respiratory timing, but to a large reduction in mean inspiratory airflow. The reduced airflow could not be attributed to alterations in pulmonary mechanics since the differences in mechanics between the groups were small. Instead, since the occlusion pressure responses to hypercapnia and hypoxia were reduced in the elderly proportionately to the ventilatory responses, reduction in neuromuscular inspiratory output was likely to be the major factor.

Adult↗
PubMed1980

Long-term vasodilator therapy with trimazosin in chronic cardiac failure.

Patients with cardiac failure have a generalized sympathetic vasoconstriction that may impair cardiac function and exercise tolerance. The ability of long-term alpha-receptor blockade and vasodilation with trimazosin (TMZ) to improve exercise capacity was studied in patients with chronic, stable heart failure of varying severity (functional exercise classes B to D). Exercise performance was monitored by respiratory gas exchange and air flow before and after patients were randomized to placebo (13 patients) or TMZ were then followed on treatment for up to 52 weeks. Significant (P less than 0.05) and sustained increases in exercise capacity, oxygen uptake, and oxygen pulse were observed with TMZ treatment in each Class B or C patient and in six of nine Class D patients, and were not observed during treatment with placebo.

Adrenergic alpha-Antagonists↗
PubMed1980

Aerobic limit of the heart perfused at constant pressure.

Autoregulatory adjustments in coronary vascular resistance (CVR) and O2 extraction (O2E) maintain O2 supply so that cardiac performance is not normally limited by O2 availability. The presence of an aerobic limit beyond which O2 availability is inadequate for the level of O2 need, however remains to be elucidated. Toward this end, 14 paced isolated canine hearts were used; coronary perfusion pressure was held constant at either 80 mmHg (8 hearts, group 1) or 40 mmHg (6 hearts, group 2). Work and O2 consumption were varied by increments in ventricular filling pressure (EDP, 16--20 mmHg) and heart rate (HR, 150--220 beats/min) and by infusion of dobutamine (D, 6--43 micrograms/min). In group 1, the aerobic limit was achieved when average EDP was 18 +/- 0.6 mmHg; HR, 181 +/- 5 beats/min; and D, 14 +/- 2 micrograms/min; CVRmin was 45 +/- 3% of control (nonworking state) and O2Emax 80 +/- 2%. Beyond this limit, additional increments in HR or D were not accompanied by further coronary vasodilatation and resulted in a marked reduction in lactate extraction (delta L/L) to -13 +/- 3%, the onset of lactate production (8 +/- 0.9 mg/100 ml), a decline in developed isovolumetric force (12 +/- 2%), and the appearance of pulsus alternans (6 hearts/. In group 2, delta L/L became negative when EDP was 19 +/- 1 mmHg; HR, 156 +/- 11 beats/min; D, 5 +/- 1 microgram/min; while O2Emax was 82 +/- 0.9% and CVR fell 13 +/- 6.6% from control; pulsus alternans appeared in 5 of these 6 hearts. We conclude that under the condition of constant coronary perfusion pressure an aerobic limit of the heart can be demonstrated. When aerobic demand exceeds O2 capacity, lactate production results, ventricular performance declines, and pulsus alternans appears.

Aerobiosis↗
PubMed1980

Alveolar response to experimental Pneumocystis carinii pneumonia in the rat.

In order to characterize the alveolar response to Pneumocystis carinii pneumonia, light and electron miscropy were used to trace the development of experimental infections with P carinii in rats treated with cortisone acetate and a low-protein diet. The first changes were found by the eighth day of treatment and consisted of the selective attachment of Pneumocystis organisms, mostly trophozoites, to alveolar Type 1 pneumocytes; the host cells were undamaged, and no inflammatory response was seen. After approximately one month of treatment, the seemingly innocuous host-parasite interaction was succeeded by focal necrosis of the Type 1 pneumocytes adjacent to organisms; hyperplasia of nearby Type 2 pneumocytes also occurred, to replace the dead Type 1 pneumocytes. Even at this stage, inflammatory reaction was conspicuously absent except for occasional alveolar macrophages in the diseased alveoli; in addition, all cells of the alveolar-capillary membrane other than Type 1 pneumocytes appeared entirely normal. Not only does the present study clarify the nature of alveolar injury caused by Pneumocystis carinii, but it also provides an experimental animal model in which selective injury of the alveolar lining cells occurs.

Animals↗
PubMed1978

Arterial PO2 and PCO2 stimulus threshold for carotid chemoreceptors and breathing.

The PaO2 and PaCO2 stimulus thresholds for activity of carotid chemoreceptors and for ventilation were investigated in twenty anesthetized adult cats at sea level. Over the range studied PaCO2 threshold for carotid chemoreceptors decreased with increasing intensity of hypoxia showing stimulus interaction. Once begun, the carotid chemoreceptor activity increased gradually at a rate that was inversely related to initial PaO2. The greater the initial hypoxia the greater was the carotid chemoreceptor activity at which the first inspiration occurred, apnea was shorter and inspiratory PaCO2 threshold lower. Hypoxia per se depressed the central mechanism for the resumption of inspiration. We conclude that (1) carotid chemoreceptor PaO2-PaCO2 stimulus thresholds are largely interdependent; (2) these receptors are activated at a lower PaO2-PaCO2 stimulus strength than ventilation is; (3) an increased input from peripheral chemoreceptors initiates breathing at a lower PaCO2 indicating that central chemoreceptor threshold is lower than the PCO2 threshold for inspiration; (4) a finite total input from the receptors is needed to start ventilation.

Animals↗